Intestines The Key To Parkinson's? - NewsChannel5.com | Nashville News, Weather & Sports

Intestines The Key To Parkinson's?

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CHICAGO ( Ivanhoe Newswire) - While a lot Parkinson's research is based on the brain, one study is focusing on an unexpected part of the body.

Richard Bailey can't play the guitar like he used to.

"I guess that's what you lose in Parkinson's is the automation," Richard told Ivanhoe.

He's taken part in several studies. The most recent was the most unusual.

"Well, it's the first time I've had a gastroenterology examine as part of a neurological exam so that was a bit of a surprise," Richard said.

Researchers at Rush University Medical Center have discovered a bad protein in the intestines that only shows up in Parkinson's patients.

Doctor Kathleen Shannon said when the protein gets to the brain, Parkinson's symptoms appear.

"If you can detect it when it's just in the intestinal wall and then prevent the spread, then patients would never have to develop typical nervous system symptoms that can cause so much disability," Dr. Kathleen Shannon from Rush University Medical Center, explained.

Doctor Jeffrey Kordower hopes the protein turns out to be a biomarker.

"Maybe we'll be able to tell who gets Parkinson's before they get Parkinson's," Dr. Jeffrey Kordower, a neurology researcher at Rush University Medical Center, said.

The goal is to develop a screening process and a treatment that attacks the protein while it's still in the intestines. Richard hopes his role in the research means an end to Parkinson's.

Doctor Shannon said the initial pilot study was small so more research needs to be done. Right now, Rush University Medical Center is recruiting for further studies.

RESEARCH SUMMARY

BACKGROUND: Parkinson's disease is a disorder in the brain which leads to shaking and difficulty with walking, movement, and coordination. Parkinson's is one of the most common nervous system disorders of the elderly and it most often develops after the age of 50, although it can sometimes occur in younger adults. Parkinson's disease occurs when the nerve cells in the brain that make dopamine are slowly destroyed, and without dopamine the nerve cells in that part of the brain cannot properly send messages leading to the loss of muscle function. Why the brain cells begin to be destroyed is unknown. (Source: www.nih.gov)

SIGNS/SYMPTOMS: The first symptoms of Parkinson's disease can be hard to diagnose, especially in older patients, and often start out mild and worsen over time. The most common signs of Parkinson's disease are shaking, called tremors, and jerky, stiff movements. Some of the other possible signs include:

  • Constipation
  • Depression, anxiety, and memory loss
  • Slowed movements, slow blinking, and slowed speech
  • Difficulty swallowing and drooling
  • Problems with balance and walking

TREATMENT: There is no known cure for Parkinson's disease and treatment is aimed at controlling the symptoms of the disease. Parkinson's patients will often times take medications, most of which increase the levels of dopamine in the brain, to control their symptoms but eventually the effects of the medication will wear off and symptoms will return. Some of the medications used to treat movement-related symptoms of Parkinson's are Levodopa, Pramipexole, Sinemet, and Amantadine. The patient may also take other medications for anything from depression to sleep disorders, as well as for pain. (Source: www.nih.gov)

NEW TECHNOLOGY: Alpha-synuclein is a protein deposited in cells of the brain in Parkinson's patients and is considered a pathologic hallmark of the disorder. The physicians from Rush University found that this same protein can be seen in the nerve cells in the wall of the intestine in patients in the early stages of Parkinson's, but the protein cannot be seen in patients without the disorder. The physicians wanted to prove that alpha-synuclein aggregates in biological tissue before the onset of motor symptoms of Parkinson's, and they are one of the first to demonstrate this. The physicians analyzed tissue samples of three patients from colonoscopies taken two to five years before the first symptoms of Parkinson's. Every sample showed the protein in the wall of the lower intestine. The hope is that this can be used as a simple early detection device for the disorder so that treatment can begin earlier and hopefully with better results. (Source: www.rush.edu)

INTERVIEW

Kathleen Shannon, M.D., Professor of Neurological Sciences at Rush University Medical Center, talks about the study that has discovered a bad protein in the intestine that only shows up in Parkinson's patients and the possible implications.

Tell me about this study. How did it come about? How did you even know there was a possible link between what is in your intestines and what is in your brain?

Dr. Shannon: Well the original idea for this came from some recent studies suggesting that the pathological changes of Parkinson's, so nerve cell loss and accumulation of protein, which we typically see in the brain in Parkinson's can also be seen in the wall of the intestine. This came from autopsy studies and it appears that the intestinal changes occur before the development of brain disease. So, we thought if we could look at living patients with Parkinson's disease and study how the intestines function and whether we could see the protein that might allow us to first learn more about the disease and then hopefully to find ways to diagnose it much earlier before the symptoms start in the brain.

What is the name of that protein?

Dr. Shannon: The name of the protein is alpha-synuclein and it was discovered in 1997 in a family of Italian and Greek Parkinson's disease patients where it was an inherited problem with the gene that controls that protein. So that is how we first started looking at that.

The protein from the studies that were done here found that it is only in people who have Parkinson's. Is that correct?

Dr. Shannon: Right. We have a small group of patients with Parkinson's disease, 10 with very early Parkinson's disease, and then we compared them to 23 people who do not have Parkinson's disease. We only found the protein in the people who do have Parkinson's disease and we found that in every one of the people with Parkinson's disease.

What could this mean? If you could catch it before it gets to the brain, could you stop it or is it a matter of treating it earlier?

Dr. Shannon: We are only able to diagnose Parkinson's disease now once it presents with certain symptoms. So a tremor or shaking of the limbs at rest, stiffness or rigidity of the limbs when you move them around, trouble with walking and balance, but we have known for a long time that our patients have other symptoms that occur before they develop these things, for example, depression and constipation. These things may signal that the disease is actually starting in parts of the nervous system that are outside the parts that produce these characteristic symptoms. We think that the early symptoms may occur up to 2 decades before the nerve symptoms first become diagnosable as Parkinson's. We have been studying for more than 20 years trying to find ways to slow disease progression in Parkinson's disease, but if it has already been going on for 20 years in the body, you are really getting in late in the game for anything that we try. So, a new focus of research is to try and identify patients before they get the shaking and slowness and stiffness. This is because if the problem is that protein is collecting in the nerve cells in the intestinal wall and then spreading to the nervous system, if you could detect it when it is just in the intestinal wall and then prevent the spread then patients would never have to develop the typical nervous system symptoms that cause so much disability. So this is kind of the future of Parkinson's disease research.

What is that protein doing inside the intestines and once it finally gets to the brain?

Dr. Shannon: Well, we know that the protein has the capability to spread from nerve cell to nerve cell. We know that this happens in the laboratory in the culture dish, for example, and we also know that it happens in real people because there are certain demonstrations of protein spread. So we know that that is happening, but what the protein is doing within the nerve cells is it starts to accumulate and create what are called aggregates which are kind of clumps of protein and then it interferes with the normal housekeeping of the cells. Cells produce their own energy and clean themselves of waste and manufacture and send various chemicals to various other places and within the cell and also into adjoining cells, so when that protein starts to accumulate, it causes those processes to go bad and eventually the cell becomes sick and dies. If that is then spreading to the next nerve cell that it is in direct communication with the cell, then that cell would become sick and die and so on until it gets to those cells that are important for movement and causes the typical movement symptoms of Parkinson's, but you can see now that this has been going on a long time before it gets to that point.

The effects of what it would do in the intestines are much different than what it would do to the brain cells?

Dr. Shannon: That is exactly right. If it causes nerve cells in the intestine to be sick and die then maybe the person has bloating or constipation or some kind of nonspecific symptom; certainly symptoms we do not consider to be neurological symptoms, but they could be. Then as it gets into the lower part of the brainstem it causes problems with sleep and depression. As it ascends up to the areas of the brain that control movement then, and only then, do we get problems with the shaking, the stiffness, and the trouble with walking and balance and that can be decades after the very first involvement of protein within the nervous system.

How excited are you about these findings?

Dr. Shannon: There are two papers that came out recently. One is this demonstration that patients with early Parkinson's disease have the protein already, but then we decided to take it one step further. Since every American is supposed to have colon screening at the age of 50 and since people with Parkinson's disease usually start on average in their late 50s, we thought well maybe there are colon biopsies in the laboratory somewhere that came from people who did not have symptoms of Parkinson's disease originally, but who then later developed them. So, our second paper looked at people who were current patients known to have Parkinson's disease, but who had biopsies taken before they developed the first sign. There are 3 cases we found in our pathology laboratory here at Rush, and they all had biopsies and then 2 to 5 years later they developed their very first symptom of Parkinson's disease. We looked at those biopsies for the protein and every single one of it; all 3 already had the protein in their intestines before they had their first symptom. Since colon tissue is easy to get, the way that we get it does not require any preparation and does not require anesthesia, it is much simpler than the traditional colonoscopy. It is possible you could identify people before they get their first symptom and if we have something that might slow disease progression, it could be much more effective if we start to treat before the symptoms begin. That is really the most important finding of these studies and it leads us to the possibility that maybe if we could find populations that have higher risks of developing Parkinson's and then screen them looking for the protein, we might be able to find those people whose future destinies might include Parkinson's disease.

How does this translate into the real world? If you get the evidence, what do you do then? What kind of treatments do you put them on or how does this affect how you would deal with the situation?

Dr. Shannon: Well, it is a different way of thinking about treatment. The current treatments have to do with trying to intervene in things that happen to nerve cells after protein deposits in the brain cells, for example. If you could prevent spread from the nerve cells in the wall of the intestines into the brain, one example of a way to do that would be to use immunization, like a vaccination. Vaccinate the body against that protein. Identify the people who have protein only in the intestines, give the vaccination, and then you could potentially prevent people from having this protein spread into the brain and cause the symptoms of Parkinson's. We need to think about it in a different way and having the ability to look at the disease much earlier allows you to have newer ways to think about treating it. I think that is also very important.

There might be a way to stop it and kind of destroy it before it reaches the brain?

Dr. Shannon: Correct, if we target spread so it does not get there in the first place instead of what happens after the protein lands in the brain cells, then I think we could have a whole different landscape of this disease; new treatments that you cannot use once the nerve cells are already affected in the brain.

How long down the road do you think we are before findings and studies are applicable and can be useful?

Dr. Shannon: I think that we are looking at the ability to test people who are at risk within the next 5 years. In fact, if adequate funding can be arranged, we could start doing that right away. I think the technology for treatments that might stop spread is in laboratories now and it would just need to be developed to the point that it could be used safely in people. For example, vaccination studies have been used in Alzheimer's disease already, so that technology is available. I would say in 5 to 10 years maybe we would be looking at potential intervention trials.

That is good news.

Dr. Shannon: That is good news.

FOR MORE INFORMATION, PLEASE CONTACT:

Deborah Song
Associate Director, Media Relations
(312) 942-0588
deb_song@rush.edu

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